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Flashcards

Lecture 8

Bella Paniagua Pathogenic Microbiology College English 95 cards

Cards in this deck (95)

  1. 1Gram ___ have more complicated, and more diverse mechanisms of secretion than Gram ____, why?-, +. because they have more complicated surface structures
  2. 2Sec System does what and requires __________?[General Secretory System]
    - posttranslationally exports unfolded proteins through the cytoplasmic membrane
    - proteins require a SIGNAL SEQUENCE
  3. 3SecBprotein chaperone
    - tetramer
    - BINDS TO SIGNAL SEQUENCE as protein exits the ribosome during translation
    - maintains the protein in an UNFOLDED STATE
  4. 4SecAATPase
    - forms a dimer
    - MOLECULAR MOTOR that powers transport
  5. 5SecYEGtranslocase complex
    - trimeric
    - forms a PROTEIN-CONDUCTING CHANNEL through the cell membrane
  6. 6Sec System - Step 11. SecB binds to the signal peptide
  7. 7Sec System - Step 22. SecB delivers the unfolded protein to a SecA-SecYEG complex
  8. 8Sec System - Step 3a, 3b3. SecA hydrolyzes ATP and pushes the protein through the pore
    3b. The signal sequence removed by signal peptidases
  9. 9Sec System - Step 44. Sequential binding of ATP and hydrolyzing of SecA to produce energy to keep pushing the protein through the SecYEG complex
  10. 10Sec system - Protein Folding Gram +protein folds as it exits the SecYEG complex
  11. 11Sec System - Protein Folding Gram -protein folds in the periplasmic space, it has to be transported across the outer membrane to get out of the cell
  12. 12TAT System (Twin-Arginine transport System) does what?transports fully folded proteins from the cytoplasm outside the cell membrane
  13. 13Which is more limited? Sec or TAT SystemTAT, because not present in all spp.
  14. 14For the TAT system, proteins contain a ___________ that targets them to the ______________.TAT signal sequence
    TAT translocase
  15. 153 Steps of TAT System1. TAT signal seq. binds to TatBC
    2. Tat pore complex formed by binding to TatA
    3. Protein is transferred through pore using PMF
  16. 16Gram - Secretion Sec-dependent systems Sec-independent systemsdependent: II, V
    independent: I, III, IV, VI
  17. 17T2SS (Type 2 Secretion System)- Sec-dependent
    - Forms a pore in the OM that is anchored to the IM
  18. 18T2SS secretes _________A-B Toxins
  19. 19T2SS Examples- ExoA from P. aeruginose (xcp system)
    - Cholera toxin from V. cholerae (eps system)
  20. 20T5SS (Type 5 Secretion System) - contains a Beta-domain that does what?- Sec-dependent
    - has Autotransporter proteins, so it transports itself
    - Beta domain: can insert into the OM and form a pore
  21. 21T5SS Steps1. Protein moves through pore to extracellular surface
    2. Remains intact as surface protein
    3. Can be cleaved to be secreted
  22. 22T5SS Examples- IgA proteases: Neisseria, Haemophilus influenzae
    - Serine protease: S. marcescens
    - VacA: H. pylori
    - Adhesin: B. pertussis
  23. 23T1SS (Type 1 Secretion System)- Sec-independent
    - Transports proteins directly from the cytoplasm to the surface
    - (one long channel between IM and OM)
  24. 24T1SS is a complex of 3 proteins:TRANSPORTER PROTEIN
    - ABC Transporter, IM transporter
    PERIPLASMIC CONNECTOR
    - connects ABC transporter to..
    OUTER-MEMBRANE PORE PROTEIN
    -usually formed from the binding of three monomers
  25. 25ABC-Transporters/T1SS- members of a protein superfamily
    - exist from prokaryotes to humans
    - well known for their abilities to transport huge variety of substances
  26. 26T1SS-like system form _________, why?- highly effective multidrug efflux systems, because they directly move stuff
  27. 27T3SS (Type 3 Secretion System)- Sec-independent
    - Toxin Injection system
    - seems to evolved from flagella assembly
  28. 28T3SS is a _______-dependent mechanism that works like a "molecular syringe" - how?- contact
    - powered by ATP when the tip binds tightly onto the host cell surface, forms an "injectisome" to penetrate other cell
  29. 29Most T3SS are ______ at both ends until when? Which causes?blocked, until they make contact with host cells
    - conformational changes on contact
    Ca2+ ion shifts due to binding --> open up channel
  30. 303 Steps of T3SS1. chaperones help translocate proteins through cytoplasmic pore
    2. effects threaded through "needle"
    3. exit the second pore formed in the host cell membrane
  31. 31T4SS (Type 4 Secretion System)- Sec-independent
    - related to conjugal-transfer (tra) systems for transferring DNA
    - proteins form tunnel-like apparatus that can directly transfer proteins or DNA into a host cell
  32. 32T4SS is a ____________, and is found in? (3 examples)- versatile transport system
    -H. pylori (cag)
    -L. pneumophila (Dot/Icm)
    -C. burnetii (Q fever)
  33. 33T6SS (Type 6 Secretion System)- Sec-independent
    - Most recently discovered secretion system
    - not as clearly defined
  34. 34T6SS is _ _ _ dependent and injection is made through _____-______ mechanisms.ATP, contact-dependent
  35. 35T6SS is found in what 5 spp.?S. enterica
    E. coli
    Y. pestis
    P. aeruginosa
    V. cholerae
  36. 36What is meant by T6SS may not be just for host cells?- also injects toxins into other bacterial cells
    - or other eukaryotic microbes
  37. 37Accessory Sec System - present in which spp.? - works similarly to ______ system, how?- Streptococcus, Staphyloccus, Listeria, Mycobacterium
    - Sec, it secretes adhesins
  38. 38CMT (Cytolysin-Mediated Translocation)- Gram + secretion system
    - found in S. pyogenes, maybe others
  39. 39T7SS (Type 7 Secretion System)- Present in mycobacteria
    - not well defined, sitll not sure how proteins transit mycomembrane
    - proteins require transport signal
    - translocation uses ATPase transporters
  40. 40Environmental conditions control expression of virulence genes in pathogens:temperature, pH, iron, Carbon, Nitrogen, cell density, osmolarity, O2/CO2
  41. 41Coordinated Regulationregulation of multiple genes in response to a particular condition or signal
  42. 42Global Regulatorwhen a single regulator controls a large number of genes and physiological processes
  43. 43Virulence genes are generally physically organized in the DNA into:- operons
    - regulons
  44. 44Operonsmultiple genes transcribed as a single mRNA and regulated by a single promoter
  45. 45Regulons- multiple genes are located in different locations in the DNA but all share a promoter region controlled by the same REGULATOR
  46. 46PrfA Regulon of Listeria MonocytogenesPrfA is a global regulator, is very efficient
  47. 47DT Expression- when iron is absent, apo-DtxR does not form a dimer and the Diphtheria toxin is produced to kill cells to help get iron
  48. 48ToxT Regulon controls transcription of ___, ___, ____, ____. and is globally regulated by ______ctxAB, tcp, acf, tag
    ToxT
  49. 49ToxT Regulon of V. cholerae i affected by several?environmental signals
    - pH, higher at slightly lower pH
    - temperature, higher at 30˙C than 37˙C
    - bile salts
    - low osmolarity
  50. 50ToxT Regulon - _______ can form dimers with _______ to activate transcriptionToxR, ToxS (ToxR/S)
  51. 51_____ is temperature regulated htpG is a ________ToxR/S
    - heat-shock protein that is actvated at temperatures above 30˙C
  52. 52Since the promoter overlaps, if htpG is being transcribed, what can't be?toxR and toxS
  53. 53What is the function of TCSs? (Two-Component Regulatory Systems)- controls many metabolic and virulence genes
    - all bacteria except Mycoplasma spp. contain some number of TCSs
  54. 54TCSs are composed of what two things?- sensor kinase
    - response regulator
  55. 55Sensor Kinase- part of TCSs
    - membrane bound proteins
    - extracellular domains sense various signals
  56. 56Response Regulator- part of TCSs
    - often transcription activators or repressors
  57. 57TCSs Example: Bordatella pertussis- BvgS (Bordatella virulence genes)
    - BvgS = complex sensor kinase
    - BvgA = response regulator that activates several operons (ptx, pts, fha, vag)
    ---> BvgAS Phosphorelay TCS
  58. 58BvgAS Phosphorelay TCS- BvgS senses temperature (higher at 37˙C), actual body signals not identified
    - phosphorelay because if there is more ways to control ON/OFF, you increase sensitivity
  59. 59Sensor Kinases often also have phophatase activity, why?- after a time, turns "offf" their cognate response regulators
    - you need a sustained signal to turn on virulence genes
  60. 60σ Factor definition- subunit of the RNA polymerase holoenzyme that allows the RNA polymerase to recognize a specific promoter
    - σ80
  61. 61Expression of different σ factors leads to...? σ factor expression can be controlled by...?- recognition of different promoters
    - different environmental conditions
  62. 62One σ factor will recognize...?- a particular set of promoters within the genome
  63. 63___ Regulates PrfA in L. monocytogenesσB
  64. 64Anti-σ factors- bind to σ factors and prevent them from being incorporated into the RNA polymerase holoenzyme
    - under stress conditions, can release σ factor they are bound to
    - can be regulated by anti-anti σ factors
  65. 65DNA Supercoiling Definition- during DNA replication or transcription, the double helix twists and causes supercoiling
  66. 66DNA Topoisomerases- can generate or relieve supercoiling to change the shape of the DNA
  67. 67Changes in supercoiling of the DNA can occur in response to...? These changes can...changes in physical condition, which cn change how accessible promoters or genes are
  68. 68DNA Supercoiling - Chlamydia trachomatis- amount of supercoiling depends on developmental cycle
    - two midcycle genes have promoters that are sensitive to supercoiling changes
  69. 69DNA Supercoiling - H. pylori- flagellar, housekeeping, and virulence genes are coordinately regulated by DNA supercoiling
  70. 70DNA Supercoiling - Shigella flexneri- virF encodes the main Tx activator of virulenc factors
    - supercoiling allows transcription by preventing H-NS transcriptional repressors from binding
  71. 71RNA Thermosensors- some RNAs for hairpin structures that unfold as temp. rises
    - the Shine-Dalgarno sequence is only accessible at high temps.
  72. 72RNA Thermosensors - Yersinia pestis- at high temps, the hairpin doesn't form and translation is high
    - at low temps the hairpin forms and translation doesn't happen
    - useful for zoonotic pathogens that move between cold and warm blooded hosts
  73. 73Quorum Sensing - autoinducers- bacteria are able to coordinate their activities as a group through small diffusable signals called autoinducers
    - bacteria can use these to sense population densities of themselves and other species to act as a group
  74. 74Quorum Sensing in Pathogenesis- production of virulence factors one a large enough population exists
    - signals when to start spreading
  75. 75Quorum Sensing in Gram - bacteria- use N-acyl homoserine lactones (AHLs) and alpha-hydroxyketones (AHKs) as signaling molecules
    - binding of AHL/AHK to it's regulator causes regulator to dimerize and then bind to promoters of target genes
  76. 76Quorum Sensing in Gram + bacteria- use autoinducing peptides (AIPs)
    - require cleavage and transport through membrane
    - once secreted, they cannot cross membranes
  77. 77Quorum Sensing Between Gram- and Gram+ Bacteria- uses autoinducer 2 (AI-2)
    - final step in production done by protein LuxS
    - Membrane difusible
    - way for bacteria to sense all other bacteria that may be growing and competing around them
  78. 78Quorum Sensing and the Agr System of Staph aureus- agr locus globally controls the expression of most virulence factors
  79. 79Staphylococci are Poor Communicators- AIPs from different staphylococcal spp. interfere with the signaling between each other
    - one species AIP may block the ability of another spp. to sense surrounding bacteria -- "blinding"
  80. 80Bacterial Interference- by supplying interfering AIPs into an organism with staph infection, you can reduce the staph infection
    - exploitable as therapeutic
  81. 81Disinfectantschemically toxic solutions that are used on nonliving surfaces
  82. 82Antisepticssubstances that are too toxic to be ingested but can be applied externally to living tissue
  83. 83Antibioticssubstances that can generally be administered internally (and externally) to the organism
  84. 84MIC Minimum Inhibitory Concentration- the minimum amount of compound needed to prevent growth of bacteria
    - the lower the MIC, the more effective the compound
  85. 85Choosing and Effective Therapeutic 1. 2. 3.1. Mechanism of action - how does it affect the bacteria, which does it work on
    2. Distribution - where can it be used, where does it work
    3. Side Effects - what are you willing to risk in order to win
  86. 86Side Effects "Differential Toxicity"- a substance is toxic to one target more than the other
    - depends on compound by compound and person to person basis
  87. 87Disinfectants & Antiseptics Mechanism of Action- work best on replicating microbes, work poorly on spores
    - chemically destroy common biological components
  88. 88Oxidizing agents...inactivate proteins and damage DNA
    - Halides, peroxides
  89. 89Metals"leaching" antimicrobials
    - copper, silver, gold
  90. 90UV Radiationdestroys DNA
    - disinfects air and surfaces, water treatment
  91. 91Phenolics- disrupt membranes
    - oxidize compounds
    - create free radicals
  92. 92Alcohols- often antiseptic on skin
    - denatures proteins
  93. 93QACs (Quaternary ammonium cations)- disrupt cell membranes
    - benzalkonium chloride
  94. 94Resistance isn't Just for Antibiotics- resistance can be developed to QACs and other compounds
  95. 95QAC resistanse- Gram- more than Gram+, LPS seems to protect outer membrane, porins prevent the QACs from diffusing to the inner membrane
    - in Gram+ there are efflux pumps

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College Pathogenic Microbiology Flashcards on Lecture 8, created by Bella Paniagua on 10/11/2015.
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Bella Paniagua
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